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Symptoms Midterm > EKG and cardiac meds > Flashcards

EKG and cardiac meds Flashcards

1
Q

What effect does the PNS have on the heart?

A

will DECREASE HR when activated via X

no effect on the blood vessels (more SNS activity)

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2
Q

What is the SNS role in the heart?

A

from Thoracic and lumbar: key for arteries and veins; causeing vasoconx to increase BP

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3
Q

What part of the brain plays big role in medulla for autonomic outlfow

A

NTS for both PNS and SNS

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4
Q

If you BP rises up really high what baroreceptors are activated? what effect does that have on the heart?

A

Increased BP will increase firing from baroreceptors–> this results in activating the SNS IHIBITORY pathway to decrease sympathetic ouflow

AND

cause EXCITAITON of PNS to lower HR

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5
Q

Where is the cell body of the vagus located?

A
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6
Q

What can influence CV status?

A

Inputsthroughcentral pathways can either excite or inhibit medullary CV centers

Emotion, pain, motor activity, etc., can influence cardiovascular status

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7
Q

What is the key pathophysciology for vasovagal syncope

A

Prolongued standing–> venous pooling and decreased venous return

+

Pain/anxiety causing sympathetic surge–> vigous cardiac contraction

=

Markedely reduced end systolic volume –> vagal reflex!

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8
Q

What is the vagal reflex

A

Bradycardia and vasodialtion leading to hypotension and syncope

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9
Q

What can you do to help person out with Bezold Jarisch reflex

A

increase fluid status, give Na tablets,

using a beta blocker can trigger event!

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10
Q

88 yo femaile feels weak and dizzy after passing the fuck out at home

Vent: 43 BPM

PR interval: 32 ms

QRS duration: 146 ms

QT/QTc: 588/497 ms

A
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11
Q

whats this shit?

A

2nd degree type 1

see prolongued PR interval until you eventually drop a beat

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12
Q

Whats the difference between type 1 and type 2 2nd degree heart block

A

Both have dropped beats

1: you see prolongued PR till drop a beat
2: you see regularly dropped beats in consistnat ratio

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13
Q

Whats this

A

3rd degree block

see inferior STEMI; characteristic tombstone appearance, the P waves beat indof PRS

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14
Q

83 yo with palpitations after syncopal episode

Vent rate: 300

PR interval: 104

QRS duration: 136ms

Pt/PTc: 132/295

A

Regular ventricular tachycardia

ventricles because the QRS is wider–> the ventricles are on loop adn beating inde of atria

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15
Q

44 yo male with hx of pychosis has syncopal episode,now assymptomatic

vent: 73

PR: 208

QRS: 96

QT/QTc: 513/565 ms

A

Prolongued QT

normal is

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16
Q

42 yo female, racing heart, syncopal episode, now asymptomatic

A

Wolf parkinson white

look for delta waves

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17
Q

What can QT prolongation lead to?

A

torsades

18
Q

Overview of EKG and ion channels

A

Key channels are:

Na

Ca

K

19
Q

What happens in phase 0 for ventricular myocyte AP

A

INa with depolarization and fast opening of Na channels as sodium rushes in!

20
Q

What happens during Phase 1 of ventricle myocyte AP?

A

(blurp at top of peak)

ITO transient and d/t K+ channel opening and K+ leaving cell

21
Q

What happens during Phase 2 (platue phase)

A

(Platue phase)

ICa-L, INaCa, IKr, IKs

key is Na and Ca are both depolarizing and have influx of + charge

this Ca+ flow is causing platue to stay depolarized

22
Q

What happens during Phase 3 of AP

A

(Repolarization phase)

IK channel open, efflux of + charge

23
Q

What’s going on in Phase 4

A

(resting phase)

Ik1, If

High K and Low Na permeability

If is our funny channel= pacemaker = SA node

24
Q

What happens if you fuck with the K+ channels?

A
25
Q

How does QT prolongation lead to torsades

A

You end up with increased chance of breaking threshold needed to stimulate beat; Ca++ channel has increased probability of getting reactivated–> causing action potential

26
Q

What is the result of a LQT1 or LQT2 from gene deletion

A

LQT1 (KCNQ1) will decrease Ks

LQT2(KCNE1) will decrease Ks

these are most prominent; we see smaller K current thus prolongation of QT bc not repolarizing as fast

27
Q

Dysfnx in LQT3 or LQT8 results in change where?

A

messes with INa (LQT3)

I(Ca) (LQT8)

in such a way to INCREASE their influx

28
Q

What are my Class I Na channel blockers

A

1A: Quinidine

2A: Lidocaine

3A: fecainide

29
Q

This drug is an anti-arrythmic works by blocking Na+ channels and K+ channels, thus causes prolongation of QT

A

Quinidine, Class 1A Na+ blocker

30
Q

This has a large effect on blocking Na+ thus decresasing depolaization but has no effect on repolarizing current or NO K+ effect

A

Flecainide

31
Q

What are the class II antiarrythmics

A

Beta blockers: propranolol

effects diastolic depolarization; most SA and AV nodes with no effect on QT prolongation

32
Q

What are my class III anti-arrythmics

A

K+ channel blockers: amiodarone and sotolol

amiodarone: can cause QT prolongation adn also inhibits Ca+ and Na+ thus it inhibts the effects QT prolongation would have so won’t see Torsades from it

Sotolo just affects K channels so do see prolongued QT

33
Q

What anti-arrythmics are concerning for causing QT pronlongation

A

Class I: quinidine and procainamide

Class 3: sotalol and amiodarone (not as concerning)

34
Q

What other drugs cause QT prolongation

A

SSRIs, antipyschotics

antibiotics: macrolides, quinolones, fungals like ketoconazole

35
Q

What ion channel changes cause QT prlongation

A

Loss of cardiac IKs, slowed delayed

Loss of function of cardiac IKr (rapidly activating delayed rectifyer)

Gain of function Cardiac Sodium

36
Q

Which drugs are okay to use on pt with symptomatic TdP?

Lidocaine

Fecainide

Metoprolol

Sotalol

A

DONT USE SOTALOL

37
Q

What is the direct effect of vagal nerve stimulation on the CV system

A

Decreases HR, no effect on force of contraction or LV and no effect on PVR

38
Q

What methods can we use to dx vasovagal syncope

A

ECG, Echocardiogrm, tilt-table test

holter monitor or implantable loop recorder

39
Q

Tx options for vasovagal syncope

A

Non pharm: pt education to avoid triggers, stay hydrated + Na+

Pharm: a1 agonist: midodrine (not great) OR B blockers and fludrocortisone better or pacemaker

40
Q

most common cause death in young athletes; see syncope in 15-25% pts. See LVH w/out loading and causes outflow obstruction.

A

Hypertrophic cardiomyopathy

41
Q

Harsh systolic mumur at apex and lower LSB

Increase murmur from squatting to stand

Passive leg elevation decreases murmur

Echo: see LV wall thick and septal hypertrophy

A

HCM

Symptoms Midterm (12 decks)

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